CHIP induces ubiquitination and degradation of HMGB1 to regulate glycolysis in ovarian endometriosis

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AI-generated summary by claude@2026-06+body, 2026-06-08

CHIP ubiquitinates and degrades HMGB1, inhibiting glycolysis and endometriosis progression, with the agonist YL-109 showing therapeutic potential.

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Abstract

Ovarian endometriosis is a common gynecological condition that can cause infertility in women of childbearing age. However, the pathogenesis is still unknown. We demonstrate that the carboxyl terminus of Hsc70-interacting protein (CHIP) is a negative regulator in the development of endometriosis and reduces HMGB1 expression in endometriotic cells. Meanwhile, CHIP interacts with HMGB1 and promotes its ubiquitinated degradation, thereby inhibiting aerobic glycolysis and the progression of endometriosis. Furthermore, the CHIP agonist YL-109 effectively suppresses the growth of ectopic endometrium in endometriosis mouse model, which could be a potential therapeutic approach for endometriosis. In conclusion, our data suggest that CHIP may inhibit the development of endometriosis by suppressing the HMGB1-related glycolysis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis HMGB1 Protein HMGB1 Protein HMGB1 Protein HMGB1 Protein HMGB1 Protein HMGB1 Protein HMGB1 Protein HMGB1 Protein

Citation neighborhood

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Cited by (33)

Source provenance

europepmc
last seen: 2026-06-18T06:15:08.409253+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-06-18T06:14:35.600070+00:00
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